MIT Exposes how Flu Virus Mutates--Just in Time for Flu Season

Research at MIT exposes how flu virus mutates by hijacking cellular mechanisms of the host cell. This news is just in time for flu season!

MIT biochemists have shed light on the mechanism that enables flu viruses to evolve so quickly, opening potential ways to slow their evolution and make more effective drugs.

We’re heading into the flu season! For flu viruses, the best time of year is when the weather’s cold and the sun is hidden behind the clouds.

Many people will see their daily activities compromised by the occurrence of a nasty cold, or worse, the flu.

It’s always difficult to make accurate predictions about which flu strains will dominate the season, but vaccination remains the most effective means of defense especially for the most vulnerable individuals.

Fatal cases are mostly people with chronic diseases such as AIDS, diabetes, cardiovascular diseases, and asthma. The flu virus, as with any aggressive external agent, can trigger decompensation. This is defined by a breakdown of the systems in the body.

Other individuals at risk are older people, morbidly obese people, and pregnant women.

Mortality rates of the seasonal flu vary from year to year because of many factors, such as the length and severity of the flu season. The effectiveness of the vaccine batches, which also varies, comes into play.

Each season, the composition of the flu shot is determined several months in advance according to the evolution of the strains of the flu virus in circulation.

Since strains can evolve and mutate in the meantime, the vaccine will be more or less effective.

How Influenza Virus Hijacks Your Cells to Evolve Faster

A team of biochemists at MIT conducted a study showing that the fast evolution of the flu virus stems in part from its ability to hijack some of the cellular mechanisms of the host cell.

The study’s findings, published in eLife, showed that the flu virus uses what’s called “chaperones”, a type of protein that helps other proteins fold and take their functional shape in order to inform its mutations.

MIT biochemists, who worked on mammalian cells infected with the H3N2virus, said that when they interfered so that viruses were no longer able to get help from host cell chaperone proteins, they did not evolve as fast as they had.

“It’s relatively easy to make a drug that kills a virus, or an antibody that stops a virus from propagating, but it’s very hard to make one that the virus doesn’t promptly escape from once you start using it,” said Matthew Shoulders, lead author of the study.

“Our data suggest that, at some point in the future, targeting host chaperones might restrict the ability of a virus to evolve and allow us to kill viruses before they become drug resistant.”

These new insights into viral evolution could potentially enhance viral treatments. There are already drugs that could be used to target chaperone proteins and inhibit their activity to slow down the virus evolution and reduce its chances of developing resistance to antivirals and vaccines.

How could these “chaperones” be involved in the same way with other deadly and rapidly-mutating viruses like HIV?

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